Loyola Pharmaceuticals Nyeri - Chemist/Pharmacy

01/11/2025

29/10/2025

Metabolic arthritis, also known as gout, is a condition characterized by the deposition of monosodium urate crystals in joints and soft tissues. This occurs due to an excess of uric acid in the blood, a condition known as hyperuricemia.

Several factors can contribute to the development of gout, including male gender, middle age (most common), a high-purine diet, alcohol consumption (especially beer), obesity, and renal impairment (which affects urate excretion). Certain medications, such as thiazides, loop diuretics, cyclosporine, pyrazinamide, ethambutol, and low-dose aspirin, can also increase the risk of gout. Additionally, genetic enzyme defects, particularly HGPRT deficiency (Lesch-Nyhan syndrome), can predispose individuals to gout.

The pathophysiology of gout involves an elevated serum uric acid level exceeding 6.8 mg/dL, which leads to the formation of urate crystals in the joints. These crystals activate neutrophils, resulting in the release of inflammatory cytokines such as IL-1, IL-6, and TNF-α, which cause acute inflammation. Recurrent attacks of gout can lead to the development of tophaceous gout and chronic arthritis.

The clinical features of gout typically include sudden and severe joint pain, often occurring at night. The first metatarsophalangeal (MTP) joint is the most commonly affected area, and the affected joint may appear red, hot, swollen, and tender, causing a sensation of “bedsheet intolerance.” In chronic gout, tophi, which are hard deposits of urate crystals, may develop on the ear helix, elbows, and Achilles tendon.

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